Download Orthopaedic Handbook

Orthopaedic
Handbook
PREPARED BY:
STANISH ORTHOPAEDIC INCORPORATED
Dr. William D. Stanish
Professor of Orthopaedic Surgery, Dalhousie University, and
Director, Orthopaedic and Sport Medicine Clinic of Nova Scotia
Halifax, Nova Scotia, Canada
March 2011
Table of Contents
OSTEOARTHRITIS...................................................... 2
LEG LENGTH INEQUALITY (Discrepancy) ........ 11
INJURIES TO THE MENISCUS OF THE KNEE .. 16
PLANTAR FASCIITIS ............................................... 21
HALLUX RIGIDUS..................................................... 26
DEGENERATIVE DISC DISEASE .......................... 33
DISORDERS OF THE ROTATOR CUFF ............... 43
PAIN............................................................................... 50
1
OSTEOARTHRITIS
Introduction
Osteoarthritis (OA) is the most common joint disorder in adults. It occurs secondary to the
deterioration of the joint (articular) cartilage. The cartilage is the material that provides
cushioning and shock absorption at the end of the bones. It also allows the joint surfaces to glide
smoothly over one another.1, 3
Osteoarthritis of the degenerative type affects the lower joints that are involved in weightbearing such as knees, hips, spine and feet. The joints of the hand that are used to grip objects
may also be affected, primarily the thumb and the index finger.2
There are basically two types of arthritis. The first type, as stated, is a degenerative type of
arthritis, usually secondary to injury, aging or mechanical disturbance.
The second type is inflammatory osteoarthritis. With inflammatory arthritis, the joint cartilage
usually deteriorates because of invasion of inflammatory by-products that damage the cartilage.
Examples are gout, psoriasis, inflammatory bowel disease and rheumatoid arthritis.
Figure 1. Severe osteoarthritis of the knee. Retrieved
January 7, 2011 from httpme.queensu.capeopledeluz
ioimagesOsteoarthritisKnee1.jpg
2
Osteoarthritis
Incidence and Prevalence
Estimating the prevalence of osteoarthritis is difficult because structural changes of the disease
may be detected by x-rays, but are not accompanied by symptoms.4
Furthermore, estimates can vary, depending on whether or not mild arthritic change within the
joint is included with moderate and severe alterations.4
The prevalence of symptomatic OA (persons with both x-ray evidence and pain) in any joint
does affect 14% of adults aged 25 and older, and 34% of those 65 years of age and older.5
From 1990 to 2005, the number of North American adults with osteoarthritis has risen by 28%.4
The prevalence of symptomatic OA in each joint is presented below.
Key Points:
Hand = 8% of adults 60 years of age or older6
Knee = 12% of adults 60 years of age or older7
Hip = 5% of adults 55 years of age or older4
Feet = 2% of adults over 15 years of age4
It is important to note that when considering x-ray evidence of osteoarthritis alone, estimates
have been as high as 80% of the population greater than 65 years of age.8
Symptomatic OA is generally more prevalent in females than males, with the exception of hip
OA4, 6, 7.
Age is an important factor in the incidence of OA.
Arthritis is uncommon in patients under the age of 40, with incidence rates increasing with age
and leveling off around 80 years of age.4, 9
It is important to note that age itself is not the sole cause of osteoarthritis.
Osteoarthritis appears more in the elderly because their load bearing joints, such as hips, knees
and feet, have been subjected to a lifetime of stress.3
A higher incidence of osteoarthritis in most joints has been linked to obesity, especially in the
knee.10, 11
3
Osteoarthritis
Excess body weight puts more stress on the weight bearing joints, increasing the wear of the
cartilage.3, 12, 13
Interestingly, non-weight bearing joints such as those in the hand have been linked with obesity,
suggesting obesity also leads to OA through other pathways.14, 15
The incidence of osteoarthritis also increases following major joint injuries and mechanical
malalignment, such as bow-legs. Repetitive joint movements, and work requiring excessive
knee bending and/or lifting, has been incriminated as provoking cartilage degeneration.16, 17
Key Points:
34% of patients, 65 years or older, have evidence of osteoarthritis.
From 1990 to 2005, the number of North American adults with osteoarthritis
has risen by 28%.
When considering x-ray evidence of osteoarthritis alone, 80% of the
population greater than 65 years of age suffers with osteoarthritis.
A high incidence of osteoarthritis has been linked to obesity, particularly in
the knee joint.
Natural History
The natural history of osteoarthritis is not well documented and not easily generalized. This is
due to the fact that the development of osteoarthritis is insidious, taking years to evolve, and the
natural history differs at the varying joint sites. The disease tends to progress most rapidly in the
finger joints and rather slowly about the knee.18
The process of osteoarthritis is characterized by progressive loss of joint cartilage, with the
secondary development of bone spurs called osteophytes.8, 19
4
Osteoarthritis
The loss of cartilage leads to a compromised joint surface, and thus the joint is unable to
effectively transfer the forces applied during daily activities. Once the joint space becomes
narrower, bone spurs will begin to form, thus increasing the surface area of the joint. This allows
the joint force to be distributed over a greater surface area.19
The pain associated with osteoarthritis is not caused by these initial changes.
The pain is a consequence of the secondary changes of the joint capsule (with distension) and
inflammation.8
These changes only start to appear after the disease has moderately progressed.
Initially the symptoms of discomfort; i.e., pain, usually come and go, and the patient will
experience exacerbations that last a few days or months.20
It has been noted that some patients have periods of months, or even years, in which they
experience little discomfort.20
The studies of the natural history of osteoarthritis demonstrate that the symptoms tend to recur;
i.e., complete remission is uncommon.
In a 15 year follow-up study, about 50% of patients with knee osteoarthritis experienced joint
deterioration, while the other 50% showed no change.21
Key Points:
The natural history of osteoarthritis is not well documented.
Osteoarthritis is characterized by progressive loss of joint cartilage.
Symptoms usually come and go, but can be subject to flare-ups that last days
or months.
Studies of the natural history of osteoarthritis show that improvement of
symptoms in the long term is extremely uncommon.
Implications
Osteoarthritis often causes functional disability and has been shown to decrease quality of life.22
Osteoarthritis causes more disability in the elderly, compared to any other disease.
The pain and psychological factors involved with OA may influence joint function, as much as
the degree of the OA present.2, 23
Patients suffering with osteoarthritis tend to avoid activities that trigger their symptoms.23
5
Osteoarthritis
Symptoms can be alleviated through medication, exercise, muscle strengthening, weight
reduction, footwear modification and the judicious use of a brace and/or walking aids.24, 25
Advanced OA may be treated through surgical means.3
It is important to note that the degree of joint pain does not always coincide with the degree of xray evidence of osteoarthritis.26
Even in very advanced cases of OA, there may be very few symptoms; i.e., of pain.
Osteoarthritis is a manageable condition. When proper interventions are taken, the resulting
limitations can be reduced, allowing the afflicted person to carry on with their daily activities.
Fig 3. X-ray images displaying front view of a normal knee (left) and an osteoarthritic knee (right) with joint space narrowing and
bony deformation. Retrieved from http://www.mendmyknee12481.com/knee_osteoarthritis_diagnosis.php on Jan 7, 2011.
Key Points:
Osteoarthritis is the most common form of joint disorder in adults.
It primarily affects the load bearing joints, such as the hips and knees.
Obesity is an important risk factor for OA, especially for the knee.
Disease onset is not well understood and is insidious.
Some patients have periods of months where they experience few symptoms.
Even in the most advanced cases of OA, there may be few symptoms present.
Treatments, both conservative and surgical, are available.
6
Osteoarthritis
Summary:
Osteoarthritis is the most common form of joint disorders in adults.
This very common disorder usually afflicts joints that have underlying mechanical
difficulties, predisposing them to early wear of the cartilage.
Advanced osteoarthritis may be treated through surgical means, but symptoms can be
alleviated by a number of non-surgical techniques; i.e., muscle strengthening, weight
reduction and walking aids.
Even in the most advanced cases of osteoarthritis, there may be but a few symptoms.
Profile - Patient #1
Forty-nine year old female presents with painful swelling about both knees and her wrists. Xrays demonstrate advanced tricompartmental arthritis.
It is noted that she has psoriatic plaques on both her elbows and both knees. She has been treated
for psoriasis since the age of twenty-three. There is also a family history of the same skin
disorder.
This patient suffers with psoriatic arthritis, which is an inflammatory condition, frequently
inherited.
Profile - Patient #2
A forty-nine year old male patient presents with pain about the medial side of the knee.
The patient’s history is that he had knee surgery at the age of eighteen. The surgery was removal
of the medial meniscus.
Clinical examination and x-ray review reveal degenerative osteoarthritis of the medial side of the
knee with a varus (bow-legged) deformity. Knee bracing is recommended.
This is the story of a person who suffers with osteoarthritis, secondary to surgical removal of the
medial meniscus, which is a common byproduct of that type of procedure.
7
Osteoarthritis
References
1.
Peyron J. 1984. The Epidemiology of Osteoarthritis. In R. Moskowitz, D. Howell, V.
Goldberg , H. Mankin. (eds) Osteoarthritis: Diagnosis and Management. Toronto,
Ontario, Canada; W.B. Saunders Company, p 9-27.
2.
Felson D. 1993. Epidemiology of Rheumatic Diseases. In D. McCarty, W. Koopman.
(Eds). Arthritis and Allied Conditions; 12th ed. London: Lea & Febiger; p 37-39.
3.
Apley G, Solomon L, Mankin H. 1993. Apley’s System of Orthopaedics and Fractures;
7th ed. London: Butterworth Heinemann.
4.
Lawrence RC, Felson DT, Helmick CG, et al. 2008. Estimates of the prevalence of
arthritis and other rheumatic conditions in the United States. Part II. Arthritis and
Rheumatism; 58: 26-35.
5.
Centres for Disease Control and Prevention. 2007-2008; National Health and Nutrition
Examination Survey. 2011.
6.
Dillon CF, Hirsch R, Rasch EK, Gu Q. 2007. Symptomatic Hand Osteoarthritis in the
United States: Prevalence and functional impairment estimates from the third U.S.
National Health and Nutrition Examination Survey; 1991-1994. American Journal of
Physical Medicine & Rehabilitation/Association of Academic Physiatrists; 86: 12-21.
7.
Dillon CF, Rasch EK, Gu Q, Hirsch R. 2006. Prevalence of Knee Osteoarthritis in the
United States: Arthritis data from the third National Health and Nutrition Examination
Survey, 1991-1994. The Journal of Rheumatology; 33: 2271-2279.
8.
Oddis CV. 1996. New Perspectives on Osteoarthritis. The American Journal of
Medicine; 100: 10S-15S.
9.
Buckwater JA, Saltzman C, Brown T. 2004. The Impact of Osteoarthritis: Implications
for research. Clinical Orthopaedics and Related Research; (427 Suppl): S6-15.
10.
Grotle M, Hagen KB, Natvig B, Dahl FA, Kvien TK. 2008. Obesity and Osteoarthritis
in Knee, Hip and/or Hand: An epidemiological study in the general population with 10
years follow-up. BMC Musculoskeletal Disorders; 9: 132.
11.
Reijman M, Pols HA, Bergink AP, et al. 2007. Body mass index associated with onset
and progression of osteoarthritis of the knee, but not of the hip: The Rotterdam Study.
Annals of the Rheumatic Diseases; 66: 158-162.
8
Osteoarthritis
12.
Segal NA, Yack HJ, Khole P. 2009. Weight, rather than obesity distribution, explains
peak external knee adduction moment during level gait. American Journal of Physical
Medicine & Rehabilitation/Association of Academic Physiatrists; 88: 180-188; quiz 189191, 246.
13.
Wearing SC, Hennig EM, Byrne NM, Steele JR, Hills AP. 2006. Musculoskeletal
Disorders Associated with Obesity: A biomechanical perspective. Obesity Reviews: An
Official Journal of the International Association for the Study of Obesity; 7: 239-250.
14.
Haara MM, Heliovaara M, Kroger H, et al. 2004. Osteoarthritis in the carpometacarpal
joint of the thumb. Prevalence and associations with disability and mortality. The
Journal of Bone and Joint Surgery. American. Vol. 86-A: 1452-1457.
15.
Brandt KD, Radin EL, Dieppe PA, van de Putte L. 2006. Yet more evidence that
osteoarthritis is not a cartilage disease. Annals of the Rheumatic Diseases; 65: 12611264.
16.
Toivanen AT, Heliovaara M, Impivaara O, et al. 2010. Obesity, physically demanding
work and traumatic knee injury are major risk factors for knee osteoarthritis - A
population-based study with a follow-up of 22 years. Rheumatology (Oxford, England);
49: 308-314.
17.
Maetzel A, Makela M, Hawker G, Bombardier C. 1997. Osteoarthritis of the hip and
knee and mechanical occupational exposure - A systematic overview of the evidence.
The Journal of Rheumatology; 24: 1599-1607.
18.
Dieppe P. 1994. Osteoarthritis: Clinical features and diagnostic problems. In J Klippel
& P Dieppe (eds). Rheumatology, Toronto, Ontario, Canada: Mosby; p 7.4.1 - 7.4.16.
19.
Klug S, Weseion G. 2000. Clinical Picture of Osteoarthritis. In J Grifka & DJ OgilvieHarris (eds). Osteoarthritis: Fundamentals and strategies for joint preserving treatment.
New York: Springer; p. 9-22.
20.
Gooberman-Hill R, Woolhead G, Mackichan F, et al. 2007. Assessing Chronic Joint
Pain: Lessons from a focus group study. Arthritis and Rheumatism; 57: 666-671.
21.
Felson DT, Zhang Y, Hannan MT, et al. 1995. The incidence and natural history of knee
osteoarthritis in the elderly. The Framingham Osteoarthritis Study. Arthritis and
Rheumatism; 38: 1500-1505.
22.
Moskowitz RW. 2009. The Burden of Osteoarthritis: Clinical and quality-of-life issues.
The American Journal of Managed Care; 15: S223-9.
9
Osteoarthritis
23.
Creamer P, Lethbridge-Cejku M, Hochberg MC. 2000. Factors associated with
functional impairment in symptomatic knee osteoarthritis. Rheumatology (Oxford,
England); 39: 490-496.
24.
Altman RD. 2010. Early Management of Osteoarthritis. The American Journal of
Managed Care; 16 Suppl Management: S41-7.
25.
Zhang W, Moskowitz RW, Nuki G, et al. 2008. OARSI recommendations for the
management of hip and knee osteoarthritis, Part II: OARSI Evidence-Based, Expert
Consensus Guidelines. Osteoarthritis and Cartilage / OARS, Osteoarthritis Research
Society; 16: 137-162.
26.
Hannan MT, Felson DT, Pincus T. 2000. Analysis of the discordance between
radiographic changes and knee pain in osteoarthritis of the knee. The Journal of
Rheumatology; 27: 1513-1517.
10
LEG LENGTH INEQUALITY (Discrepancy)
Leg length inequality (LLI), as the name implies, is a disorder characterized by different leg
lengths.
The discrepancy between legs can vary from less than a centimeter to over 20 cm. - which has
been published. Leg length inequality can cause asymmetry of forces on the spine, hips and
knees.1
Figure 1. Rear view of pelvic tilt and spinal
curvature caused by severe leg-length
discrepancy. Retrieved from
www.cbppatient.com on Feb 18, 2011.
Incidence and Prevalence
Leg length inequalities are quite common in the population.
Up to 93% of children have LLI.2
These discrepancies generally correct themselves during growth or by surgical options.1
In adults, prevalence of leg length inequality has been estimated as high as 40 to 70% of the
general population. 2, 3
Most leg length discrepancies are 2 cm or less and thus are not considered clinically significant
in an adult.1
11
Leg Length Inequality
Only 1 out of every 1000 people has a leg length inequality of over 2 cm.4
Total hip replacement surgery, which is a common procedure, can cause LLI.4, 5
In fact, over 25% of patients undergoing this surgery have resulting leg-length discrepancy.4
Key Points:
Most leg-length discrepancies are 2 cm or less and are not considered
clinically significant in an adult.
Only 1 out of every 1000 patients has been estimated to have a leg length
discrepancy of over 2 cm.
Natural History
Leg length inequalities typically result during childhood growth. Disruptions of the growth plate
can result from trauma and/or from disorders affecting the growth plates. Most large
discrepancies can be corrected or diminished before adulthood.1
The kinetic chain is composed of the lower limbs and spine. If there is a disruption in the chain,
as with leg length inequality, joints and muscles are placed under abnormal stresses during
stance and movement.6
Leg length inequalities have been implicated in a variety of disorders, including low back pain,
scoliosis and hip and knee osteoarthritis.6, 7
Research has shown individuals who acquire leg length inequality at a younger age are able to
better compensate for the discrepancies than those who acquire leg length inequalities later in
life. More demanding adults, such as athletes, are more sensitive to leg length inequalities
compared to less active individuals, due to the greater amount of force placed on their
musculoskeletal systems.6
Key Points:
Leg length inequalities typically result during childhood growth.
Leg length discrepancies have been implicated in a variety of disorders,
including low back pain.
Implications
As mentioned previously, most leg length inequalities are resolved or diminished during
childhood growth.
12
Leg Length Inequality
Small leg length discrepancies are quite common in adults, but the effects are reduced by the
compensatory abilities of the kinetic chain.
Leg length inequalities under 2 cm are believed to have limited significance, as individuals tend
to compensate with other joints and muscles.1
Studies have shown that walking patterns are essentially unchanged with small leg length
inequalities.8 Therefore, no treatment is usually needed for discrepancies that are 2 cm or less.1
Athletes and active individuals may have increased sensitivity to small leg length inequalities
and may require treatment.6
For leg length inequalities that cause symptoms, foot lifts are a simple and excellent treatment.
Such lifts have been shown to restore normal function and effectively reduce symptoms, such as
hip and low back pain.1, 6, 9
In leg length inequalities over 5 cm, foot lifts are poorly tolerated.
If the length discrepancy is very severe, surgery may be necessary.
Key Points:
Leg length inequalities under 2 cm are believed to have limited significance.
Athletes and active individuals may have increased sensitivity to small leg
length inequalities.
Foot lifts are a simple and excellent treatment.
Summary
Leg length inequalities can cause asymmetry and pain in the joints of the lower limbs
and in the spine.
In the adult population, the prevalence of leg length inequalities have been estimated as
high as 70%.
Most leg length inequalities are 2 cm or less and thus the body can readily compensate.
Most athletes and active individuals are typically more sensitive to leg length
inequalities than inactive individuals.
Foot lifts are a simple and effective treatment for reducing pain and improving
function.
13
Leg Length Inequalities
Profile - Patient #1
A sixty-five year old female patient underwent a total hip replacement for severe arthritis in her
right hip.
Post-operatively she did well, except for developing considerable low back discomfort. It was
noted that her corrected extremity was now 3 cm longer than her non-operated side.
A shoe lift balanced her hips and her spine, alleviating the discomfort.
Profile - Patient #2
A fifty-eight year old male had previous surgery to his right knee, resulting in considerable
osteoarthritis and marked varus deformity (bow-legged). The absolute leg length discrepancy
was 3 cm.
Following total knee replacement, the patient was given a straight leg and thus balanced the
surgical knee, bringing the leg lengths back to a normal compensated position; i.e., both leg
lengths were equalized.
References
1.
Moseley CF. 2006. Leg Length Discrepancy. In: Morressy RT, Weinstein SL, editors.
Lovell and Winter’s Pediatric Orthopaedics; 6th ed. Philadelphia, PA: Lippincott
Williams & Wilkins.
2.
Subotnick SI. 1981. Limb Length Discrepancies of the Lower Extremity (the short leg
syndrome). The Journal of Orthopaedic and Sports Physical Therapy; 3: 11-16.
3.
Woerman AL, Binder-MacLeod SA. 1984. Leg Length Discrepancy Assessment:
Accuracy and precision in five clinical methods of evaluation. The Journal of
Orthopaedic and Sports Physical Therapy; 5: 230-239.
4.
Gurney B, Mermier C, Robergs R, Gibson A, Rivero D. 2001. Effects of limb-length
discrepancy on gait economy and lower extremity muscle activity in older adults. The
Journal of Bone and Joint Surgery. American Volume; 83-A: 907-915.
5.
Canadian Institute for Health Information. 2009. Hip and Knee Replacements in Canada
- Canadian Joint Replacement Registry (CJRR) 2008-2009 Annual Report.
6.
Gurney B. 2002. Leg Length Discrepancy. Gait & Posture; 15: 195-206.
14
Leg Length Inequalities
7.
Golightly YM, Allen KD, Renner JB, et al. 2007. Relationship of Limb Length
Inequality with Radiographic Knee and Hip Osteoarthritis. Osteoarthritis and
Cartilage/OARS, Osteoarthritis Research Society; 15: 824-829.
8.
Gofton JP, Trueman GE. 1971. Studies in Osteoarthritis of the Hip. II. Osteoarthritis of
the Hip and Leg Length Disparity. Canadian Medical Association Journal; 104: 791-799.
9.
Golightly JP, Tate JJ, Burns CB, Gross MT. 2007. Changes in pain and disability
secondary to shoe lift intervention in subjects with limb length inequality and chronic low
back pain: A preliminary report. The Journal of Orthopaedic and Sports Physical
Therapy; 37: 380-388.
15
INJURIES TO THE MENISCUS OF THE KNEE
Introduction
The knee menisci are two cartilage wedges that work in conjunction within the joint to perform
vital function.
Basically, the knee menisci work as shock absorbers, providing cushions between the thigh bone
(femur) and the shin bone (tibia).
Further, the menisci provide an element of stability within the knee joint 1, 2, as the knee moves
front to back and side to side. Also, they provide an element of stability when the knee rotates or
pivots.
Therefore, the knee menisci are under stress in all everyday activities. The meniscus can tear
under several situations, most commonly when the knee is bent and then rotated.
Incidence and Prevalence
There are two distinct types of injuries to the meniscus.
Type #1 - A Traumatic Tear
This normally occurs in a younger population and is a result of excessive force placed on the
meniscus. Maneuvers that place load on the meniscus, when the knee is bent and then rotated,
lead to the most common mechanism of injury.5 Pivoting maneuvers in soccer, basketball,
wrestling and skiing are most common.3
16
Injuries to the Meniscus of the Knee
Type #2 - Degenerative Tears
This type of tear is most prevalent in the older population and results from cumulative stress on
the meniscus.3 Such degenerative tears are not uncommon in those individuals who have
associated degenerative arthritis of the joint cartilage.
Tears of the meniscus are more common in males than in females, with the ratio ranging from
2.5:1 to 4:1. The incidence of traumatic tears of the meniscus is about 60 to 70 cases per
100,000 people, peaking in men between 20-30 years of age. For both sexes, degenerative tears
become more common after the age of 303. Degenerative tears are most prevalent amongst the
elderly. One study found that 76% of people with an average age of 65 years, and without knee
pain, had x-ray evidence of a tear of the meniscus.4
Key Points:
Meniscal tears may be traumatic or degenerative.
Degenerative tears are more prevalent in older people.
Most degenerative tears are accompanied by osteoarthritis on the adjacent
joint surfaces.
76% of patients, with an average age of 65 years, have evidence of a meniscal
tear radiographically.
Natural History
The natural history of meniscal tears is variable, depending on the location, size and type of tear.
As previously mentioned, injuries of the meniscus can result from either a single traumatic event,
which most commonly occurs in the younger population, or degeneration within the meniscus.
Meniscus tears can be asymptomatic or they can be accompanied by varying degrees of pain,
swelling and catching within the knee 5. Degenerative tears occur in the meniscus that lose their
elasticity with age and as mentioned, are often accompanied with knee osteoarthritis 6, 7. These
degenerative tears can occur from routine activities and may very well remain asymptomatic
throughout life 3.
17
Injuries to the Meniscus of the Knee
Tears can vary in size, shape and orientation, resulting in a variety of symptoms and treatment
strategies 8. Minor tears of the meniscus are usually left alone, whereas larger tears, which are
usually post traumatic, are treated with surgical repair or a partial excision. Both of these
techniques are done arthroscopically in a minimally invasive fashion.
Key Point:
Small tears of the meniscus can be left alone, without treatment, and do not
lead to progressive osteoarthritis.
Implications
Both traumatic and degenerative meniscal tears can be asymptomatic or they can cause
symptoms of pain, swelling and/or locking. The treatment of meniscal tears depends on several
factors: the location, size, age, symptoms and quality of tissue 10. If the tear causes symptoms,
there are minimally invasive surgical techniques to preserve as much of the meniscus as possible
and relieve the symptoms 7, 11, 12, 13. Degenerative meniscal tears with associated osteoarthritis
rarely require surgery.
Key Point:
If the patient requires surgery, the goal is to preserve as much meniscus as
possible, thus reducing the risk of developing post surgical osteoarthritis.
Summary
There are two types of meniscal tears: traumatic and degenerative.
Meniscal tears are often asymptomatic and may never require treatment.
Traumatic tears are more prevalent in young people, whereas degenerative tears are
more common in people over 30 years of age.
Meniscal tears are more common in men.
Minor/small tears are stable and can be left untreated.
Treatment depends on size, shape, location, symptoms and quality of the tissue.
Surgical treatments usually result in returning to an active lifestyle, particularly if the
meniscal tear is post traumatic.
18
Injuries to the Meniscus of the Knee
Profile - Patient #1
Twenty-eight year old male twists his knee while stepping down from a ladder. The patient feels
immediate pain on the inside of the knee and has difficulty extending the knee. This patient
complains that the knee feels locked, and also complains of slight swelling.
This is a typical story of a vertical traumatic tear of the meniscus, with a piece of the cartilage
locked in the joint - a so-called Bucket Handle tear of the meniscus. This situation is rectified
with arthroscopic surgery, which is designed to repair the meniscus tear or remove the unstable
fragment.
Patient #2
A fifty-eight year old male patient complains of pain on the inside of the knee. The pain is
aggravated by jogging and deep squatting. The patient has mild bow-legness and the MRI
reveals a medial meniscus tear with early osteoarthritis.
This is a typical story of a degenerative medial meniscus tear, with associated early degenerative
arthritis of the medial compartment.
Initially this patient is treated with mild pain medication, physiotherapy and a knee brace.
References
1.
Messner K, Gao J. 1998. The Menisci of the Knee Joint. Anatomical and functional
characteristics, and a rationale for clinical treatment. Journal of Anatomy. 193 (Pt 2):
161-178.
2.
Wojtys EM, Chan DB. 2005. Meniscus Structure and Function. Instructional course
lectures. 54: 323-330.
3.
Brockmeier S, Rodeo S. 2009. Meniscal Injuries. In: DeLee J, Drez D, Miller M,
editors. DeLee and Drez’s Orthopaedic Sports Medicine; 3rd ed. Electronic: Saunders.
4.
Bhattacharyya T, Gale D, Dewire P, et al. 2003. The clinical importance of meniscal
tears demonstrated by magnetic resonance imaging in osteoarthritis of the knee. The
Journal of Bone and Joint Surgery. American Volume. 85A: 4-9.
5.
Arendt L. 2009. Acute Knee Injuries. In: Brukner P, Khan K, editors. Clinical Sports
Medicine; 3rd ed. London: McGraw-Hill.
6.
Brady OH, Hurson BJ. 2000. Acute Injuries of the Meniscus. In: Harries M, Williams
C, Stanish WD, Micheli LJ; editors. Oxford Textbook of Sports Medicine; 2nd ed. New
York: Oxford University Press Inc., p 441.
19
Injuries to the Meniscus of the Knee
7.
Englund M, Guermazi A, Lohmander LS. 2009 The Meniscus in Knee Arthritis.
Rheumatic Diseases, Clinics of North America; 35: 579-590.
8.
Starke C, Kopf S, Petersen W, Becker R. 2009. Meniscal Repair. Arthroscopy: The
Journal of Arthroscopic & Related Surgery. Official Publication of the Arthroscopy
Association of North America and the International Arthroscopy Association. 25: 10331044.
9.
Arnoczky SP, Warren RF. 1982. Microvasculature of the Human Meniscus. The
American Journal of Sports Medicine. 10: 90-95.
10.
Jarit GJ, Bosco JA. III. 2010. Meniscal Repair and Reconstruction. Bulletin of the NYU
Hospital for Joint Diseases. 68: 84-90.
11.
Sgaglione NA, Steadman JR, Shaffer B, Miller MD, Fu FH. 2003. Current Concepts in
Meniscal Surgery: Resection to Replacement. Arthroscopy: The Journal of North
America and the International Arthroscopy Association. 19 Suppl 1:161-188.
12.
Fairbank TJ. 1948. Knee Joint Changes after Meniscectomy. The Journal of Bone and
Joint Surgery. British Volume. 30B: 664-670.
13.
Salata MJ, Gibbs AE, Sekiya JK. 2010. A systematic review of clinical outcomes in
patients undergoing meniscectomy. The American Journal of Sports Medicine; 38: 19071916.
20
PLANTAR FASCIITIS
Plantar fasciitis is a common source of heel pain. It is generally caused by overuse, which can
occur under many circumstances - including modified footwear, excessive walking, standing or
walking on a different terrain.
The plantar fascia is a bridge of tissue that extends from the heel to the front of the foot, on the
underside. It is generally under significant resting tension in order to provide shock absorption
and maintain proper arches in the foot.
Excessive stress on the plantar fascia can lead to inflammation and pain on the underside of the
heel.
Incidence and Prevalence
It has been noted that as many as 1 in 10 people will develop plantar fascia in their lifetime 1. It
can occur at any age, but is more prevalent among those 40-60 years of age. Common risk
factors for plantar fasciitis include increased body weight and abrupt change in challenges to the
plantar fascia with standing or walking. Certain foot types are commonly observed with
individuals suffering with plantar fasciitis. Most typically the patient has a high-arched foot, pes
cavus deformity or a mobile flat foot pes planus.
21
Plantar Fasciitis
Key Points
Common risk factors include:
Increased body weight.
Abrupt excessive challenge and/or change in terrain.
Pes cavus and pes planus are commonly seen in patients who suffer with
plantar fasciitis.
Natural History
Plantar fasciitis is generally a self-limiting disease, whereby 80% of cases can be expected to
resolve on their own within a year. Non-surgical treatments, such as physiotherapy, the use of
orthotics and the intermittent use of anti-inflammatory medications lead to resolution in 90% of
cases.
Usually time alone will resolve the problem. Surgical intervention is rarely necessary.
Key Point:
22
80% of cases can be expected to resolve on their own within a year.
Implications
Plantar fasciitis is a bothersome disorder that can be resolved, in most cases, with non-surgical
treatment. Generally the challenge in resolving plantar fasciitis lies in the willingness of the
patient to allow the tissue to heal, understanding that the natural history of the problem is that it
is usually self-limiting. Healing involves resting the affected area and limiting the challenges
that have provoked the problem initially. To reiterate, the problem is usually self-resolving and
very rarely requires surgical intervention.
Plantar Fasciitis
Key Points
Most cases resolve with a conservative program.
Summary
Plantar fasciitis is a very common source of foot pain.
It is usually caused by overuse of the foot with a rapid change in challenges such as
standing, walking or running.
Symptoms can usually be resolved with conservative treatment alone.
Profile - Patient #1
A thirty-eight year old nurse, who is overweight, develops heel pain when she prompts herself to
adopt a weight reduction program. This weight reduction program includes walking 10 km a
day. Further, she was using a new pair of rather rigid walking shoes.
23
She experienced pain on the front part of her heel. The remainder of her physical examination
and x-ray review was normal.
This is a typical story of a person who develops acute plantar fasciitis, which is a reflection of an
exercise program that was too strenuous for the deconditioned plantar fascia.
The patient was placed on a program of physiotherapy, with a heel sponge, coupled with weight
reduction and the problem resolved after six months.
Profile - Patient #2
A twenty-four year old male developed heel pain when ramping up his exercise program.
Physical examination revealed a very high-arched foot with distinct tenderness over the heel.
The problem resolved with a custom-made orthotic, combined with physiotherapy and an antiinflammatory medication.
This is a typical story of a person who has an underlying anatomical problem related to their
longitudinal arch of the foot, and makes them quite prone to developing plantar fasciitis and/or
Achilles tendinitis.
24
Plantar Fasciitis
References
1.
Riddle DL , Schappert SM. Volume of ambulatory care visits and patterns of care for
patients diagnosed with plantar fasciitis: A national study of medical doctors. Foot and
Ankle Int. 2004; 25(5): 303-310.
2.
Buchbinder R. Clinical Practice: Plantar Fasciitis. N Engl J Med 2004. 20;350(21):
2159-2166.
3.
Davis PF, Severud E, Baxter DE. Painful Heel Syndrome: Results of non-operative
treatment. Foot and Ankle Int. 1994; 15(10): 531-535.
25
HALLUX RIGIDUS
Hallux rigidus, which means “stiff big toe,” is an arthritic condition that affects the first joint of
the big toe. This joint is called the metatarsophalangeal joint.
Essentially the condition is osteoarthritis of the joint which results from deterioration of the joint
cartilage. Secondarily, bone spurs around the joint then form.
The degeneration of the joint can range from mild to severe and likewise the symptoms
associated with hallux rigidus can range from mild to disabling.
On examination, the joint becomes enlarged (secondary to bone spur formation). There is
usually associated inflammation and joint stiffness. Upon movement by the practitioner, there is
reduced range of motion and pain, if the toe is moved aggressively.
Hallux rigidus is seen in two distinct populations. Persons may present in adolescence and
invariably have a family history of this condition.
The second population is those who present in adulthood.1, 2
Figure #1: x-ray showing osteoarthritis of
the joint - hallux rigidus
26
Hallux Rigidus
Key Points
Hallux rigidus is an arthritic condition of the first metatarsophalangeal joint.
Stiffness of the joint is the paramount finding.
The degree of degeneration and restricted range of motion may be mild,
moderate or severe.
Hallux rigidus may appear in adolescence and in the more aged population.
Incidence and Prevalence
Hallux rigidus is the most common arthritic condition affecting the feet and the second most
common condition of the big toe, second only to Hallux valgus (bunions).2, 3
There is contradicting information regarding the gender distribution of hallux rigidus, with
multiple studies suggesting an increased prevalence existing with females 4, 6 while others cite a
greater prevalence amongst males 7, 8.
As with most arthritic conditions, the prevalence of hallux rigidus appears to increase with age.
It has been estimated that 10% of people aged 20-34 have evidence on x-ray of the condition.
Upwards of 44% of people over the age of 80 years of age have radiographic features of hallux
rigidus.
It has been reported that for younger people the incidence of hallux rigidus increases with a
history of hyperextension injuries or by repeated stubbing of the big toe.9, 10
In a recent major literature review, it was estimated that between 6.3 and 39% of the population
have hallux rigidus; however, the majority of the studies were making this diagnosis by x-ray
alone.11
It has been previously estimated that between 2 and 3% of the population have symptomatic
hallux rigidus.12
In upwards of 80% of cases of hallux rigidus, the problem is in both feet.13
Key Points
44% of patients over the age of 80 years have x-ray evidence of hallux
rigidus.
It remains unclear as to whether trauma can produce hallux rigidus,
particularly when there has been no evidence of fracture.
27
In upwards of 80% of cases, the problem is bilateral; i.e., involves both feet.
Hallux Rigidus
Natural History
Hallux rigidus is a chronic, degenerative disorder. It can develop due to a traumatic injury to the
joint (specifically when there has been evidence of a fracture of the joint) or as a result of
progressive degeneration of the joint cartilage. Unfortunately, due to the nature of articular
cartilage (poor innervation, poor vascular supply), once degradation begins, the process
continues as cartilage has no ability to heal.14
Damage and degeneration of the cartilage weakens its structure, resulting in the inefficient
transmission of force within the joint. With the loss of cartilage, the space within the joint
becomes narrower and the surface of the bone can become exposed, devoid of cartilage.
Secondarily, bone spurs commence to form and the joint becomes more rigid.2, 14
Pain is usually noticed most with extremes of movement of the joint. By the time the threshold
of pain has been reached and the patient begins to present with symptoms of hallux rigidus, there
is usually significant degeneration and wear of the joint surface, but such is not always the
case. 2, 14
The degree of wear of the joint does not always coincide with the degree of degeneration.
The pain produced by movement of the joint is typically made worse with loading of the joint
(weight bearing activities). This may lead to the patient walking with a limp in an effort to
reduce the pain. The natural progression usually results in complete fusion of the joint, but the
pain can be reduced through bracing and/or surgery.2, 14
Key Points
Hallux rigidus is a chronic degenerative disorder.
It may be painful with activity.
The degree of pain does not always coincide with degree of degeneration.
Implications
The natural course of this disorder is loss of the articular cartilage of the joint, joint space
narrowing, and bone spur formation on the first metatarsophalangeal joint. This may cause pain
with activities sufficient to impair quality of life and activities of daily living. During the early
stages, the symptoms can be adequately controlled by activity modification. For example,
refraining from high heeled shoes and avoiding high impact activities such as running on ones
toes. Additionally, patients in the early phase may benefit from the use of stiff soled shoes.2
28
Hallux Rigidus
Figure #2: Hallux Rigidus at SurgeryComplete loss of cartilage
Hallux rigidus has been shown to be manageable through non-surgical procedures. A study by
Smith et al (2000) found that although there was radiographic evidence of further degeneration
of joint space, 90% of patients surveyed stated that their pain had not changed 15 years after their
diagnosis.15 The indication for surgical intervention with hallux rigidus is an unacceptable level
of pain with associated disturbance of daily activities. Surgical options include debridement of
the spurs of the joint. More aggressive surgery options include arthrodesis (fusion of the joint)
or synthetic joint replacements. The results from such surgical interventions are highly
successful and are tailored for the individual patient.
Summary
Hallux rigidus is a common arthritic condition affecting the first metatarsophalangeal
joint of the big toe.
Hallux rigidus is a chronic, degenerative condition that results in pain and reduction of
mobility of the big toe.
It has been estimated that 2 to 3% of the population are afflicted with hallux rigidus.
Hallux rigidus is effectively managed through conservative measures; in severe cases,
surgical interventions have been shown to improve symptoms and restore motion.
29
Hallux Rigidus
Patient Profile #1
A twenty year old male presents with pain and limitation of motion of the great toe. Physical
examination reveals enlargement of the toe and reduced range of motion. The patient claims
discomfort when the great toe is forcibly moved. X-rays reveal degeneration of the first
metatarsophalangeal joint, compatible with osteoarthritis; i.e., hallux rigidus. The patient is
markedly improved with the use of a rigid walking shoe.
Patient Profile #2
A sixty year old female presents with pain and limitation of motion of the first
metatarsophalangeal joint. It is first noticed when she walks in a shoe with an elevated heel. Xrays reveal evidence of early osteoarthritis of the first metatarsophalangeal joint; i.e., hallux
rigidus. Attempts at modification of her footwear do not improve her circumstance, but she does
become asymptomatic after a minor surgical debridement of the joint.
30
Hallux Rigidus
References
1.
Gould J. (1993). Painful Feet. In D. McCarty & W. Koopman (Eds), Arthritis and Allied
Conditions; 12th edition (pp 1553-1561). London: Lea & Febiger
2.
Michelson J. (2007) Lower Extremity Considerations: Foot and Ankle. In RW
Moskowitz, RD Altman, MC Hochberg, JA Buckwater & VM Goldberg (Eds),
Osteoarthritis: Diagnosis and medical/surgical management; 4th edition (pp 415-425).
Philadelphia: Lippincot Williams & Wilkins.
3.
Gilheany MF, Landorf KB, & Robinson P. (2008) Hallux valgus and hallux rigidus: a
comparison of impact on health-related quality of life in patients presenting to foot
surgeons in Australia. Journal of Foot and Ankle, 1:14-19
4.
Bremner JM, Lawrence JS, Miall WE. (1968) Degenerative Joint Disease in a Jamaican
Rural Population. Ann Rheum Dis., 27(4): 326-332
5.
Solomon L, Beighton P, Lawrence JS. (1976) Osteoarthritis in a Rural South African
Negro Population. Ann Rheum Dis., 35(3): 274-278
6.
Van Saase JL, van Romunde LK, Cats A, Vandenbroucke JP, Valkenburg HA. (1989)
Epidemiology of Osteoarthritis: Zoetermeer Survey. Comparison of radiological
osteoarthritis in a Dutch population with that in 10 other populations. Ann Rheum Dis.
48(4) 271-280.
7.
Brighton SW, de la Harpe AL, van Staden DA. (1985) The prevalence of osteoarthritis in
a rural African Community. Br J Rheumatol, 24(4): 321-325
…/6
Wilder FV, Barrett JP, Farina EJ. (2005) The association of radiographic foot
osteoarthritis radiographic osteoarthritis at other sites. Osteoarthritis Cartilage, 13(3):
211-215
8.
9.
Gilmore MFX. (1987) The overuse syndromes. In S Hughes, M Benson, C Colton (Eds),
Orthopaedics: The principles and practice of musculoskeletal surgery and fractures (pp
232-243). New York: Churchill Livingstone.
10.
Bentley G. (1987) Surgical management of osteoarthritis. In S. Hughes, M Benson, C
Colton (Eds), Orthopaedics: The principles and practice of musculoskeletal surgery and
fractures (pp 120-151). New York: Churchill Livingstone.
11.
Triveldi B, Marshall M, Belcher J, Roddy E. (2010) A systematic review of radiographic
definitions of foot osteoarthritis in population based studies. Osteoarthritis & Cartilage,
18: 1027-1035.
31
Hallux Rigidus
12.
Gould N, Schnider W, Ashikaga T. (1980) Epidemiological survey of foot problems in
the continental United States, 1978-1979. Foot and Ankle, 1: 9-10.
13.
Coughlin MJ, Shurnas PS. (2003) Hallux rigidus: demographics, etiology, and
radiographic assessment. Foot and Ankle Int, 24(10): 731-743.
14.
Poole AR, Guilak F, Abramson SB. (2007) Etiopathogenesis of osteoarthritis. In RW
Moskowitz, RD Altman, MC Hochberg, JA Buckwater & VM Goldberg (Eds),
Osteoarthritis: Diagnosis and medical/surgical management, 4th edition (27-49).
Philadelphia: Lippincott Williams & Wilkins.
15.
Smith RW, Katchis SD, Ayson LC (2000) Outcomes in hallux rigidus patients treated
nonoperatively: A long-term follow-up study. Foot and Ankle Int, 21(11): 906-913.
32
DEGENERATIVE DISC DISEASE
There is no standard definition for degenerative disc disease (DDD). It has been suggested that
DDD be defined as “an aberrant, cell-mediated response to progressive structural failure”.1
Although an exact definition is unclear, the term degenerative disc disease is widely used to
describe changes in spine anatomy that are part of the normal aging process.
The vertebrae form a motion segment connected by intervertebral discs, joints, ligaments and
muscles
Figure 1 – The different sections of the spine (available from:
http://boneandspine.com/spine/thoracic-lumbar-spine/lumbarspinemorphologic-functional-anatomy/
The discs act like spacers and flexible connectors. The muscles produce movement and the
ligaments prevent excessive movement.
The intervertebral discs change with age. We do not know what starts the process or exactly
what influences its progression.
In the earliest stage of degeneration, small tears appear in the outer part of the disc and the inner
part of the disc begins to dry out.
These changes start fairly early in life.
33
Degenerative Disc Disease
Figure 2 – The motion segment includes two
vertebrae, the disc and joints between them, and the
ligaments and muscles that connect them (available at:
msd.com.mx)
The disc starts to lose some of its shock absorbing ability. This process lets the vertebrae slide,
resulting in segmental instability and putting more pressure on the joints.
Over time, arthritis will occur in those joints, thus eventually stiffening the spine and rendering it
less mobile.
Figure 3 – Degenerative changes in the spine (available at:
http://www.oispine.com/subject.php?pn=lumbardegenerative-disc-002)
34
Degenerative Disc Disease
The process is similar to degenerative arthritis in other joints, such as the hip and knee.
Tears in the outer part of the disc usually result from wear and tear over a period of time - the
accumulation of many small injuries. Most injuries result from compressing the disc with a
combination of a twisting motion, especially while bending forward. Tears can also weaken the
outer ring and thus allow the inner nucleus pulposus of the disc to bulge outward through the
weakened ring and sometimes herniate completely.
The large bulges can cause pain that is felt in the buttock and leg. Herniations can sometimes
press on the nerve roots exiting from the spine, causing weakness and numbness.
Figure 4 – Tears in the outer part of the disc can let the inner nucleus
pulposus bulge outward against, or even through, the outer rings.
Theses bulges can press on nerve roots, but also can cause pain just
by stretching the annulus fibrosus.
Key Points
There is no standard definition for degenerative disc disease.
The intervertebral discs change with age.
With aging of the disc, the joints of the spine become overloaded and can
develop a secondary osteoarthritis.
The casing of the disc may tear, resulting in a protrusion of the central nucleus
pulposus.
Incidence and Prevalence
Degenerative changes occur in the disc by late adolescence, increase linearly with age and occur
in nearly 100% of people by old age.
Degenerative changes are extremely common in the neck, as well as the lower back, and so
increase with aging.
35
Degenerative Disc Disease
Over 60% of people have degenerative changes in their cervical spine by age forty, and even
25% of those younger than age forty also show degenerative changes.
In the lumbar spine the numbers are even higher, whereby tears in the discs start when people are
in their twenties. By age seventy, 75% to 98% of people have degenerative disc disease.
Low back pain affects 20% of the population on any given day, and upwards of 80% of people
experience low back pain.
Low back pain is the most common musculoskeletal complaint and the second most common
complaint of pain to headache, which ranks number 1.
Many people with degenerative disc disease do not experience pain.
We cannot predict who will have back pain based on the presence of degenerative changes of the
disc that are visible on x-rays and/or MRI.
Figure 5 – X – rays do not show the intervertebral discs,
but changes can be inferred from the altered spatial
relationships between adjacent vertebral bodies.
(available at:
http://bookmasters.com/markplc/rr00941.htm
36
Figure 6 – Degenerative changes of the lumbar spine,
including disc bulging at the L-3/4, L-4/5 and L-5/S-1
discs. Degeneration of the nucleus pulposus results in
the discs appearing darker than those above, with no
central lighter area. These changes are common, and
are not accompanied by low back pain in most
people.13
Available at:
http://emedicine.medscape.com/article/95294overview
Degenerative Disc Disease
Key Point
Degenerative disc disease is common and does not necessarily cause back or
neck pain. 20% of the population suffers with low back pain on any given
day, and upwards of 80% of people experience low back pain during their
lifetime.
Risk Factors for Low Back Pain
Since degenerative disc disease alone does not cause pain, it is unclear why some people develop
low back pain and others do not. Age, smoking and genetic factors (as yet unknown) seem to be
the strongest risk factors for developing low back pain.2 Getting older increases the chances of
developing low back pain, as well as degenerative disc disease. Heavy lifting, vibration, driving,
prolonged postures - all of these have been described as risk factors for low back pain, but the
evidence linking these factors to causing degenerative disc problems is tenuous. In fact, both
increased and decreased loading can contribute to DDD.20
Risk factors, then, may increase the symptoms of low back pain, but do not appear to cause an
increase in degenerative changes in the spine. Low back pain probably comes from a
combination of changes in the spine, genetic factors, and loading patterns.1, 2
Implications and Natural History
Degenerative disc disease is not really a disease at all, but a normal part of the aging process.
Changes begin in adolescence or early adulthood in men, about a decade later in women, then
progress linearly until old age. There is an interesting phenomenon in as much as low back pain
becomes less frequent and less severe with age.
90% of the people who experience low back pain for the first time, get better in two to six weeks.
Only about 5% of people with low back pain develop chronic low back problems; e.g., pain
lasting longer than six months.
Since degenerative disc disease is a normal aging process, no treatment is required if there is no
pain present or it is mild.
Treatments should be divided into non-surgical and surgical options, although the latter is
required for only a few people.
Non-surgical treatments can involve medications, exercise, weight loss, physiotherapy and low
back education.
37
Degenerative Disc Disease
Certainly, all treatment for low back pain should include education about the process and the
lack of association between degenerative disc disease and the low back pain.
Healthcare professionals should encourage the patient to stay as active as possible because rest
does not change the overall course of recovery for low back pain.
Key Points
Treatment for back and neck pain should always include education that
degeneration is normal and does not necessarily cause pain.
Advised to exercise and stay as active as possible.
Reassurance is necessary that pain is not equal to harm.
38
Reassurance that most people get better in a few weeks.
Addendum
Types of Back Pain
Annular Tears & Internal Disc Disruption
This type of problem is usually caused primarily by multiple small tears in the annulus,
prompting mechanical back pain and secondary inflammation.
The treatment is postural retraining, exercises and anti-inflammatory medications.
Disc Protrusions and Herniations
Even normal discs can be injured. Heavy repetitive bending, twisting or lifting can place too
much pressure on the disc, tearing some fibers and making it weaker.5, 15, 20
A large disc herniation, that is resistant to non-surgical measures, may require surgical treatment.
Facet Joint Arthritis
With degeneration of the disc, the facet joints become arthritic.
In such patients, manipulation or joint mobilizations 9 can be helpful, coupled with reduction in
body weight.
39
Degenerative Disc Disease
Summary
Degenerative disc disease is a natural part of the aging process and affects everyone
eventually.
Treatment for low back pain can be quite successful if it is tailored to the patient’s
condition.
Surgery is seldom necessary, except in cases of large disc herniations.
Patient Profile #1
Twenty year old male complains of acute low back pain while lifting. He presents with
significant paravertebral spasm, but no evidence of any sciatic nerve root irritation; however,
there is limitation of motion about the lumbar spine.
This gentleman presents with a classic story of a small tear of the annulus surrounding the central
part of the disc. The inflammatory process has triggered paravertebral spasm, but without any
evidence of nerve root pressure.
This patient is treated non-surgically with anti-inflammatory medication, reduction in activities
and physiotherapy program using passive modalities. He is back to work in three weeks.
Patient Profile #2
A sixty-two year old female presents with recurrent episodes of low back pain. On physical
examination the patient is overweight, with a pendulous abdomen and x-ray evidence of
degenerative disc disease at L4-L5. There is no evidence of any neurological deficit.
This patient suffers with mechanical back pain as a consequence of degenerative disc disease and
facet joint osteoarthritis.
This situation is treated without surgery but with enhanced fitness, weight reduction, postural
retraining and education regarding low back care.
40
Degenerative Disc Disease
References
1.
Adams MA, Roughley PJ. What is intervertebral disc degeneration, and what causes it?
Spine, 2006; 31(18): 2151-2161
2.
Battie MC, Videman T, Parent E. Lumbar disc degeneration. Epidemiology and genetic
influences. Spine, 2004; 29(23): 2679-2690
3.
Binder AI. Cervical spondylosis and neck pain. BNJ; 2007; 334: 527-531
4.
Boden SD, et al. Abnormal magnetic-resonance scans of the crevical spine in
asymptomatic subjects. A prospective investigation. JBJS, 1990; 72-A(8): 1178-1184
5.
Bogduk N. Clinical anatomy of the lumbar spine and sacrum, Third Edition. Churchill
Livingstone, 1997
6.
Burton K et al. The Back Book: the Best Way to Deal with Back Pain; Get Back Active.
TSO (The Stationary Office)
publishers, 2002, available at:
http://www.tsoshop.co.uk/bookstore.asp
7.
Friedendberg ZB, Miller WT. Degenerative disc disease of the cervical spine: a
comparative study of asymptomatic and symptomatic patients. JBJS, 1963; 45-A(6):
1171-1178
8.
Gross DP, et al. A population-based survey of back pain beliefs in Canada. Spine, 2006;
31(18): 2142-2145
9.
Hebert J, Koppenhaver S, Fritz J, Parent E. Clinical prediction for success of
interventions for managing low back pain. Clin Sports Med, 2008; 27(3): 463-479
10.
Hicks GE, Morone N, Weiner DK. Degenerative disc and facet disease in oder adults:
prevalence and clinical correlates, Spine; 34(12): 1301-1316
11.
Long A, Donelson R, Fung T. Does it matter which exercise? A randomized controlled
trial of exercise for low back pain. Spine 2004; 29:2593-602
12.
Maetzel A, Li L. The economic burden of low back pain: a review of studies published
between 1996 and 2001. Best Practice & Research Clinical Rheumatology, 2002; 16(1),
23-30
13.
Malanga GA, Eisenberg ME. Degenerative lumbar disc disease in the mature athlete.
Downloaded Jan. 20, 2011 from: http://emedicine.medscape.com/article/95294-overview.
14.
Martin MD, Boxell CM, Malone DG. Pathophysiology of lumbar disc degeneration: a
review of the literature. Neurosurg Focus, 2002; 13(2): 1-6
41
Degenerative Disc Disease
15.
McGill S. Low back disorders: evidence-based prevention and rehabilitation, 2nd edition.
Human Kinetics, 2007
16.
McKenzie R, May S. The lumbar spine. Mechanical Diagnosis and Therapy, Spinal
Publications, 2003
17.
Okada E, et al. Aging of the cervical spine in healthy volunteers. Spine, 2009; 34(7):
706-712
18.
Perez C. Chronic back problems among workers. Health Reports, 2000; 12(1): 41-55,
Statistics Canada, Catalogue 82-003
19.
Richardson CA, Jull G, Hodges PW, et al. Therapeutic exercise for spinal segmental
stabilization in low back pain. London: Churchill Livingstone, 1999
20.
Stokes IA, Iatridis JC. Mechanical conditions that accelerate intervertebral disc
degeneration: overload vs immobilization. Spine, 2004; 29(23): 2724-2732
21.
Wilkins K. Incident arthritis in relation to excess weight. Health Reports, 2004; 15(1):
39-49. Statistics Canada, Catalogue 82-003
42
DISORDERS OF THE ROTATOR CUFF
The shoulder is the most mobile and unstable joint in the body. The four rotator cuff
muscle/tendon units aid in shoulder movements and also stabilize the joint.
Due to the large complex movements of the shoulder joint, injuries of the rotator cuff are quite
common.1
Fig1. Front and back views of the four muscles
that compose the rotator cuff. Retrieved on
January 24, 2010 from
http://www.physicaltherapystretchingexercises.
com/wp-content/uploads/2010/05/b3.jpg
Incidence and Prevalence
The prevalence of rotator cuff injuries has been well documented. It is reported that more than
50% of individuals older than 60 years of age have at least a partial thickness rotator cuff tear.2
Rotator cuff tears typically develop from natural degeneration of tendons and as a result,
prevalence does increase with age.3-6
The incidence of rotator cuff tears rises sharply after the age of 50.7
Athletes and labourers, especially those that use overhead arm motion, have higher incidence of
rotator cuff disruptions.1 Tears of the rotator cuff in younger individuals generally result from
traumatic shoulder injuries, but are quite uncommon.
Sher et al reported only 4% of individuals 19-39 years of age had a tear of the rotator cuff.5
43
Disorders of the Rotator Cuff
It is important to note that many rotator cuff tears are asymptomatic, even when the tears are full
thickness.5, 8
One study has shown that 26% of people, with an average age of 44 years, had radiographic
evidence of at least partial rotator cuff tear despite having no symptoms.8
Another study reports 7.6% of individuals, between the ages of 50-79 years, had full-thickness
tears which were asymptomatic.
Key Points:
50% of people over the age of 60 years have rotator cuff pathology.
Full tears of the cuff may be asymptomatic.
44
Overhead workers are at increased risk.
Natural History
Degeneration is the most common cause of rotator cuff tears. In degenerative rotator cuff
disruptions, the tendons weaken with age and even routine activities can cause injury in the
elderly.
Other factors can accelerate the degenerative process, such as impingement of the tendons
between the bones of the shoulder joint or from repetitive overhead shoulder movements in the
athletes or labourers.
Traumatic rotator cuff tears are far less common and typically result from an acute shoulder
injury, such as shoulder dislocations or acromioclavicular joint separations.1
Fig 2. Computer-generated image of a rotator cuff tear in the right shoulder. Retrieved on January
24, 2011 from http://www.sportsmd.com/SportsMD_Articles/id/262/n/torn_rotator_cuff.aspx
45
Disorders of the Rotator Cuff
Disease progression has not been well studied. One study found that 50% of asymptomatic tears
had developed into symptomatic tears over 5 years. They also found that 36% of the tears
increased in size.9
Another study demonstrated that pain development in asymptomatic tears is associated with an
increase in the size of the tear.10
Another important finding is that very few rotator cuff tears actually heal or decrease in size over
time.9, 11, 12
The aforementioned studies on progression provide some evidence that untreated rotator cuff
tears have a good chance of progressing in symptoms and size.
Larger tears are associated with decreased strength 4 and increased pain.4, 6 Chronic tears can
progress and become very large in size, being referred to as “massive” rotator cuff disruptions.
In such a case, the humeral head migrates up, causes further impingement and leading to joint
arthritis.13
Key Points:
Degeneration is the most common cause of cuff tears.
Acute trauma is far less common in triggering rotator cuff tears.
Untreated tears may progress in size and symptoms.
Implications
It is important to note that up to 75% of rotator cuff tears are asymptomatic and the presence of
tearing should not be the sole guide to treatment.1, 14 Many individuals with full thickness tears
can have normal functioning with no pain.6
In most cases, symptomatic rotator cuff tears should be treated conservatively.15 Physiotherapy,
flexibility and strengthening exercises have been found to improve shoulder function, allowing
individuals to perform daily activities.14, 15 Conservative treatment has proven especially
effective in the elderly where there is a reduced need for a strong shoulder.16
It is important to note that conservative treatment does not heal the tear. The goal is to improve
the function of the healthy tissue around the tear.15
When conservative treatment is ineffective, surgical options can be considered.1 Surgical
decisions are based on level of symptoms, level of physical activity, size of tear, quality of tissue,
and response to conservative treatment.15 For example, surgery is generally recommended for
younger individuals with a traumatic tear, because they will likely have healthy tissue, a good
chance of healing, and typically require higher shoulder function than older patients.1, 16
46
Disorders of the Rotator Cuff
Summary
Degenerative rotator cuff tears are very common in the elderly; more than 50% of 60
year olds.
The incidence of rotator cuff tears increases with age, rising sharply after 50 years.
Many tears are asymptomatic - 26% of 44 year olds have tears with no symptoms.
Individuals with full-thickness tears can still have full function of the shoulder.
Conservative treatment is highly effective, especially in the elderly.
Surgical options exist when conservative treatment is ineffective.
Profile - Patient #1
A thirty-eight year old truck driver slips on the threshold of his truck, grabs on to the rearview
mirror and has a severe pain in his shoulder.
Upon presentation, he is unable to move the shoulder away from his side beyond 25 degrees.
The MRI of the shoulder reveals a complete tear of the rotator cuff. Within three weeks of
injury, the patient undergoes surgery to repair the rotator cuff disruption.
Six months after the repair he is back to full and unrestricted duties.
This is a typical story of an acute rotator cuff tear in a relatively young person, that responds best
to a surgical program.
Profile - Patient #2
A seventy-three year old gentleman suffers with pain about his right shoulder, when he fell in his
garden on his outstretched arm.
He had a history of intermittent shoulder pain, dating back for fifteen years.
On examination, his range of motion is 90 degrees of forward elevation.
An MRI of the shoulder reveals a tear of the rotator cuff, with retraction and evidence chronic
impingement.
This patient responded well to a physiotherapy and exercise program, designed to strengthen his
complimentary muscles.
47
Disorders of the Rotator Cuff
Five months after the injury the patient is functioning fine, with a range of motion of 140 degrees
and he has returned to all his daily activities, including gardening and golf.
This is a typical story of a chronic rotator cuff problem, with an acute injury in a more geriatric
patient. Most patients in this age group respond best to a conservative, non-surgical program.
References
1.
Lin KC, Krishnan SG, Burkhead WZ. 2009. Impingement Lesions in Adult and
Adolescent Athletes. In: DeLee J, Drez D, Miller M, editors. DeLee and Drez’s
Orthopaedic Sports Medicine; 3rd Ed., Saunders.
2.
Wolf BR, Warme BA, Kibler WB, Sciascia A, Kuhn JE. 2009. Non Acute Shoulder
Injuries. Knowledge Update: Sports Medicine, American Academy of Orthopaedic
Surgeons; p 19-39.
3.
Milgrom C, Schaffler M, Gilbert S, vanHolsbeeck M. 1995. Rotator cuff changes in
asymptomatic adults. The effect of age, hand dominance and gender. The Journal of
Bone and Joint Surgery; British Volume; 77: 296-298.
4.
Moosmayer S, Smit HJ, Tariq R, Larmo A. 2009. Prevalence and characteristics of
asymptomatic tears of the rotator cuff: An ultrasonographic and clinical study. The
Journal of Bone and Joint Surgery. British Volume; 91: 196-200.
5.
Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB. 1995. Abnormal findings on
magnetic resonance images of asymptomatic shoulders. The Journal of Bone and Joint
Surgery; American Volume; 77: 10-15.
6.
Yamaguchi K, Ditsios K, Middleton WD, et al. 2006. The demographic and
morphological features of rotator cuff disease. A comparison of asymptomatic and
symptomatic shoulders. The Journal of Bone and Joint Surgery. American Volume; 88:
1699-1704.
7.
Christian C. 1998. Shoulder and Elbow Injuries. Campbell’s Operative Orthopaedics,
9th Ed. Toronto, Ontario, Canada: Mosby
8.
Reilly P, MacLeod I, MacFarlane R, Windley J, Emery RJ. 2006. Dead Men and
Radiologists Don’t Lie: A review of cadaveric and radiological studies of rotator cuff tear
prevalence. Annals of the Royal College of Surgeons of England; 88: 116-121.
9.
Yamaguchii K, Tetro AM, Blam O, et al. 2001. Natural history of asymptomatic rotator
cuff tears: A longitudinal analysis of asymptomatic tears detected sonographically.
Journal of Shoulder and Elbow Surgery / American Shoulder and Elbow Surgeons...[et
al] 10: 199-203.
48
Disorders of the Rotator Cuff
10.
Mall NA, Kim HM, Keener JD, et al. 2010. Symptomatic progression of asymptomatic
rotator cuff tears: A prospective study of clinical and sonographic variables. The Journal
of Bone and Joint Surgery. American Volume; 92: 2623-2633.
11.
Yamanaka K, Matsumoto T. 1994. The joint side tear of the rotator cuff. A follow-up
study by arthrography. Clinical Orthopaedics and Related Research. (304): 68-73.
12.
Maman E, Harris C, White L, et al. 2009. Outcome of non-operative treatment of
symptomatic rotator cuff tears monitored by magnetic resonance imaging. The Journal of
Bone and Joint Surgery. American Volume; 91: 1898-1906.
13.
Goldstein J, Zuckerman JD. 2000. Selected orthopaedic problems in the elderly.
Rheumatic Diseases Clinics of North America; 26: 593-616.
14.
Mantone JK, Burkhead WZ, Jr., Noonan J, Jr. 2000. Non-operative treatment of rotator
cuff tears. The Orthopaedic Clinics of North America; 31: 295-311.
15.
Smith MA, Smith WT. 2010. Rotator cuff tears: An overview. Orthopaedic Nursing /
National Association of Orthopaedic Nurses; 29: 319-322; quiz 323-324.
16.
Williams GR, Jr., Rockwood CA, Jr., Bigliani LU, Iannotti JP, Stanwood W. 2004.
Rotator Cuff Tears: Why do we repair them? The Journal of Bone and Joint Surgery.
American Volume; 86-A: 2764-2776.
49
PAIN
Introduction on Pain
The official definition of pain, as described by the International Association for the Study of Pain
is “an unpleasant sensory and emotional experience associated with actual or potential tissue
damage”.1
Pain is highly variable, having symptoms depend on the degree, type, duration, and location of
the stimulus. Interpretation of pain depends on the person’s subjective experience and
consequently, there are no objective measures of pain.1, 2 It is important to note that pain is an
important protective biological function that acts as a warning signal of tissue damage or
potential damage.2
Source of
Pain Pain signal
Fig 1. Diagram of simple pain reflex.
is sent to central nervous system (Spinal Cord and
brain) where pain is interpreted and reflex signal is
sent to leg muscles
In order to properly understand the concept of pain, one must understand the physiological
components of the nervous system associated with pain. A painful stimulus (mechanical,
thermal, or chemical) acts on specialized pain receptors called nociceptors. Nociceptors then
transmit the signal to the central nervous system, where the pain signal is interpreted.2 For
example (Fig. 1), when someone steps on a sharp object, the nociceptors in the damaged skin
transmit signals to the central nervous system, causing a reflex which lifts the foot off the sharp
object. Finally, the brain interprets the type and degree of pain. This is an example of acute
pain, which is a relatively simplistic model and the pain generally subsides. However, chronic
pain is typically more complicated and often involves other confounding variables which may
include psychological distress, obesity, social support and smoking.
50
Pain
Key Points:
Interpretation of pain depends on the person’s subjective experience.
There are no objective measures of pain.
Chronic Pain Syndrome
Chronic pain is defined as pain lasting longer than 3 months. It develops from an acute injury,
degenerative tissue, or a systemic illness and is most commonly located in the back, head, and
joints.2, 3 Chronic pain causes substantial direct and indirect economic costs, primarily by work
absence.2
After an acute injury, it is unknown why some individuals develop chronic pain while other get
better. Studies have identified several risk factors that increase the likelihood of developing
chronic pain including: depression, stress, anxiety, smoking, obesity, sleep disturbance, and poor
social support.2 There is evidence that the nervous system gets rewired after the injury causing
the pain receptors to become more sensitive.4 When pain lasts longer than 3 months, it is likely
to persist for at least 12 months.2
In patients seeking chronic pain management, approximately 50% had psychological distress
such as depression and/or anxiety. Psychological distress increases both the development and
the persistence of chronic pain. Psychological treatment should be addressed when managing
persistent pain.2 The prevalence of chronic pain in the general population has been estimated at
46-48%.5, 6
Clearly, a corresponding percentage of the population is not disabled, indicating pain and
function can be effectively managed.3
Three important categories of chronic pain are summarized below including: chronic low back
pain, central nervous system pain, and peripheral nervous system pain.
Fig 2. The above diagram highlights the complexity chronic pain. Psychological distress increases
the likelihood of developing chronic pain, and in turn, can cause the symptoms to persist.
51
Pain
Key Points:
In patients seeking chronic pain management, approximately 50% have
psychological distress, such as depression and/or anxiety.
52
The prevalence of chronic pain in the general population has been
estimated at 48%
1) Chronic Low Back Pain
Low Back Pain (LBP) is the most common type of chronic pain.2 Approximately 80% of
the world’s population will develop low back pain at some point in their adult life.7 Most
chronic LBP is mechanical and develops after acute low back pain injuries.8 The majority
of acute low back pain incidents improve within a few weeks 9 but approximately 20%
develop into persistent symptoms, resulting in work absence. This group is responsible
for a disproportionate (80%) of low back pain related costs.10
Fig 3. Low back pain is the most common type
of chronic pain. Retrieved on Feb 14, 2011
from www.severelowerbackpain.net/
Similar to most chronic pain problems, there is limited knowledge to identify which acute
low back injuries progress to chronic episodes. There are several pre-existing factors that
have been shown to increase the likelihood of developing persistent pain including:
psychological conditions, poor coping strategies, poor general health, smoking, obesity,
age, and persons that catastrophize or exaggerate pain.11
Chronic low back pain treatment should incorporate medication, physiotherapy, exercise,
psychological, and social strategies.12, 13 Patients should not expect complete pain
resolution but proper treatment can effectively control pain and improve function.13
Pain
2) Central Nervous System Pain
The central nervous system (CNS) is composed of the brain and spinal cord. One of the
primary functions of the CNS is integrating and processing sensory information from the
53
body, including pain. Central nervous system pain develops from lesions caused by
traumatic injury or disease. CNS lesions result from a variety of disorders which may
include traumatic brain and spinal cord injuries, strokes, tumors, multiple sclerosis, and
Parkinson’s disease. CNS pain is caused by heightened pain sensitivity and is often
described as burning, aching, or pricking.14, 15 It is important to note that not all lesions
produce CNS pain.14
At least 8% of stroke patients are affected by CNS pain.16 35-40% of traumatic spinal
cord injury patients and 30% of Multiple Sclerosis patients suffer from CNS pain.15, 17
Treatment of central and peripheral nervous system pain depends on the ability to treat
the underlying condition. Pharmaceutical options do not typically provide sufficient
relief.14
Fig 4. Fig 4. Central and peripheral nervous systems. CNS is
composed of the brain and spinal cord. PNS is composed of
the peripheral nerves. Retrieved on Feb 14, 2011 from
http://reasonablywell-julia.blogspot.com/
3) Peripheral Nervous System Pain (Peripheral Neuropathy)
The peripheral nervous system (PNS) is composed of all other parts of the nervous
system lying outside the brain and spinal cord. The role of the PNS is relaying messages
to and from the central nervous system, including pain. As mentioned above,
“nociceptors” are pain receptors that detect harmful or potentially harmful stimuli, which
are then transferred along the spinal nerves to the central nervous system for processing.2
54
Pain
Peripheral neuropathy typically results from damage to the nociceptors or spinal nerves
by toxic, metabolic, traumatic, or autoimmune pathways. Symptoms typically begin at
the feet and gradually move up the body. Common symptoms include numbness, loss of
temperature
detection, “burning” sensations, tightness, and tingling. Peripheral neuropathy can also
affect the
motor pathways, affecting muscle weakness, loss of proprioception, painful muscle
cramping, sweating, and even major organ function.18 There are too many different
causes of peripheral neuropathy to describe in detail but the most common types will be
described below.
i) Diabetic peripheral neuropathy affects 47% of individuals with diabetes.19
Prevalence increases with age, duration of diabetes and being male.20 Symptoms can be
controlled by tight regulation of blood-sugar levels, reducing weight, physical activity,
and ceasing smoking.2
ii) Alcoholic neuropathy results from a lifetime of excessive alcohol consumption.
Neuropathic symptoms are observed in 25-66% of alcoholics.21 Recovery is possible if
alcohol consumption is discontinued.22
iii) Carpal tunnel syndrome (CPS) - Bones and ligaments of the wrist form the
carpal tunnel. Muscle tendons and the median nerve pass through the carpal tunnel.
Swelling of muscle tendons can compress the median nerve, causing carpal tunnel
syndrome. Symptoms include burning, tingling, numbness, and muscle weakness in
areas of the hand and wrist. The prevalence rate of CPS in the general population is
higher in women (5.9%) than in men (0.6%). Conservative treatment can improve
symptoms but when ineffective, surgical options are effective.23
Chronic Pain Summary
Chronic pain can be caused by acute injuries, degenerative tissue, or systemic
illnesses.
After an acute injury, it is unknown why some develop chronic pain and others
do not.
Psychological distress and other health factors increase the likelihood of
developing chronic pain.
The prevalence of chronic pain in the general population has been estimated at
46-48%. Clearly, a corresponding percentage of the population is not disabled,
indicating pain and function can often be effectively managed.
Chronic low back pain is the most common type of chronic pain.
55
Pain
Central and peripheral nervous system disorders are important causes of chronic
pain.
Treatment of central and peripheral nervous system pain primarily depends on
the ability to treat the underlying condition.
Profile – Patient #1
A thirty-eight year old female has a minor injury to her left elbow when she bumps her
arm against a filing cabinet.
She reports immediate severe pain to her employer.
examination are normal.
Initial x-rays and physical
After two years, she continues to complain bitterly of pain about her left elbow. She has
been unable to return to the workplace.
On physical examination the arm is held in a protected position. The skin is glossy. The
range of motion of the finger joints are reduced and the hair, as well as her fingernails
have overgrown.
This is a classic story of an individual suffering with a chronic pain syndrome, secondary
to a regional dystrophy after an episode of minor trauma.
Profile – Patient #2
A forty-eight year old sanitary engineer injures his neck and upper back in a low energy
motor vehicle collision. He complains of pain in his neck and his shoulders, which fails
to respond to physiotherapy, medications and time away from the workplace.
Eighteen months later he remains unemployed. All investigations are normal. He is seen
by his neighbors playing baseball with his children, shopping for groceries and
gardening.
This is a classic story of a person with chronic low back pain. There is no objective
evidence of disease. The patient complains of chronic difficulties.
56
Pain
References
1.
International Association for the Study of Pain. 2011
2.
Marcus DA. 2009. Chronic Pain: A primary care guide to practical management.
2nd Ed. New York: Humana Press; 442 p.
3.
Gureje O, VonKorff M, Simon GE, Gater R. 1998. Persistent Pain and WellBeing: A World Health Organization study in primary care. JAMA: The Journal
of the American Medical Association; 280: 147-151.
4.
Voscopoulos C, Lema M. 2010. When does acute pain become chronic? British
Journal of Anaesthesia; 105 Suppl 1: i69-85.
5.
Torrance N, Smith BH, Bennett MI, Lee AJ. 2006. The Epidemiology of
Chronic Pain of Predominantly Neuropathic Origin. Results from a General
Population Survey. The Journal of Pain: Official journal of the American Pain
Society. 7:281-289.
6.
Elliott AM, Smith BH, Penny KI, Smith WC, Chambers WA. 1999. The
Epidemiology of Chronic Pain in the Community. Lancet 354: 1248-1252.
7.
Anderson GB. 1997. Low Back Pain. Journal of Rehabilitation Research and
Development; 34: ix-x.
8.
Nachemson A. 1976. Current Topics on Backache. Lakartidningen 73: 1304.
9.
Pengel LH, Herbert RD, Maher CG, Refshauge KM. 2003. Acute Low Back
Pain: Systematic review of its prognosis. BMJ (Clinical Research ed.) 327: 323.
10.
Waddell G. 2004. The Back Pain Revolution, 2nd ed. Edinburgh: Churchill
Livingston
11.
Chou R, Shekelle P. 2010. Will this patient develop persistent disabling low back
pain? JAMA: the Journal of the American Medical Association; 303: 1295-1302.
12.
Heitz CA, Hilfiker R, Bachmann LM, et al. 2009. Comparison of risk factors
predicting return to work between patients with subacute and chronic non-specific
low back pain: Sysematic Review. European Spine Journal: official publication
of the European Spine Society, the European Spinal Deformity Society, and the
European Section of the Cervical Spine Research Society; 18: 1829-1835.
13.
Diamond S, Borenstein D. 2006. Chronic Low Back Pain in a Working-Age
Adult. Best Practice & Research. Clinical Rheumatology; 20: 707-720.
57
Pain
14.
Wasner G. 2010. Central Pain Syndromes. Current Pain and Headaches Reports;
14: 489-496.
15.
Osterberg A, Boivie J, Thuomas KA. 2005. Central Pain in Multiple Sclerosis Prevalence and Clinical Characteristics. European Journal of Pain (London,
England) 9: 531-542.
16.
Schott GD. 1996. From Thalamic Syndrome to Central Post-Stroke Pain.
Journal of Neurology, Neurosurgery, and Psychiatry; 61: 560-564.
17.
Siddall PJ, McClelland JM, Rutkowski SB, Cousins MJ. 2003. A longitudinal
study of the prevalence and characteristics of pain in the first 5 years following
spinal cord injury. Pain; 103: 249-257.
18.
Cooper G, Eichhorn G, Rodnitzky RL. 2008. Peripheral Neuropathy. In: Conn
PM, editor. Neuroscience in Medicine, 3rd ed. New Jersey: Humana Press.
19.
Dyck PJ, Kratz KM, Karnes JL, et al. 1993. The prevalence of staged severity of
various types of diabetic neuropathy, retinopathy, and nephropathy in a
population-based cohort: The Rochester Diabetic Neuropathy study. Neurology;
43: 817-824.
20.
Veves A, Backonja M, Malik RA. 2008. Painful Diabetic Neuropathy:
Epidemiology, natural history, early diagnosis and treatment options. Pain
Medicine (Malden, Mass); 9: 660-674.
21.
Laker SR, Sullivan WJ. 2008. Alcoholic Neuropathy. 2010.
22.
Fields H, Baron R, Rowbotham M. Peripheral Neuropathic Pain: An approach to
management. In: Wall P, Melzack R, editors. Textbook of Pain, 4th ed. Toronto,
Ontario, Canada: Churchill Livingstone; p 1523-1533.
23.
Zhao M, Burke D. 2008. Median Neuropathy. In: Frontera W, Silver J, Rizzo T,
editors. Essentials of Physical Medicine and Rehabilitation, 2nd ed. Saunders.
58